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Gibberellin signaling regulates pectin biosynthesis in Arabidopsis

Author

Listed:
  • Yan Xu

    (Qingdao New Energy Shandong Laboratory)

  • Jinge Du

    (Qingdao New Energy Shandong Laboratory
    University of Chinese Academy of Sciences)

  • Ruili Hao

    (Qingdao New Energy Shandong Laboratory)

  • Siqi Ma

    (Institute of Chinese Academy of Agricultural Sciences)

  • Yujiao Ma

    (Qingdao New Energy Shandong Laboratory)

  • Gongke Zhou

    (Qingdao Agricultural University)

  • Ruibo Hu

    (Qingdao New Energy Shandong Laboratory
    Shandong Agricultural University)

  • Shengjun Li

    (Qingdao New Energy Shandong Laboratory
    Shandong Agricultural University)

Abstract

Pectin is an abundant polysaccharide with essential roles in various biological processes. Despite considerable advances in understanding the regulatory mechanisms of pectin biosynthesis, the influence of phytohormones on this process remains unclear. Here we report that gibberellins (GA) promotes pectin biosynthesis in Arabidopsis. The DELLA proteins, as GA signaling repressors, interact with TRANSPARENT TESTA GLABRA2 (TTG2) and components of the MYB-bHLH-WD40 (MBW) complex, the key regulators of pectin biosynthesis, to repress their transcriptional regulatory activities. Furthermore, the MBW proteins and TTG2 physically interact and synergistically activate the downstream target GLABRA2, whereas this interaction and collaboration are competitively attenuated by DELLAs. Genetic analyses validate that GA-mediated pectin biosynthesis relies on functional TTG2 and MBW proteins. Moreover, the pectin biosynthesis mediated by the GA-DELLA-MBW-TTG2 module contributes to GA-regulated seedling growth. Our findings reveal the significance of the GA-DELLA-MBW-TTG2 signaling cascade in the regulation of pectin biosynthesis and plant development.

Suggested Citation

  • Yan Xu & Jinge Du & Ruili Hao & Siqi Ma & Yujiao Ma & Gongke Zhou & Ruibo Hu & Shengjun Li, 2025. "Gibberellin signaling regulates pectin biosynthesis in Arabidopsis," Nature Communications, Nature, vol. 16(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-59268-2
    DOI: 10.1038/s41467-025-59268-2
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